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Although the effects of angiotensin II receptor blockers (ARBs) on non-diabetic glomerulonephritis have been reported, studies of their effects on collagenvascular diseases, particularly lupus nephritis, are limited. In this retrospective, observational study, systemic lupus erythematosus (SLE) patients ( n = 7) with lupus nephritis and uncontrolled proteinuria were treated with an angiotensin-converting enzyme inhibitor followed by the ARB losartan (25–50 mg/day). Urinary protein excretion and renal function were evaluated. After 12 months of losartan, mean urinary protein excretion decreased significantly by 84.8%. Mean systolic and diastolic blood pressures also decreased significantly during the 12 months of losartan treatment, although not in normotensive patients. Complement 4, total complement activity and anti-dsDNA antibody levels, which are indices of SLE activity, and serum creatinine levels, which is an index of renal function, showed no change in response to losartan treatment. A more extensive evaluation of the effects of ARBs in patients with lupus nephritis and poorly controlled proteinuria is required.

A 65-year-old Japanese woman was diagnosed in 1996 with a pathological fracture of the left femur caused by immunoglobulin D-type myeloma (IgD myeloma). She responded well to combination chemotherapy followed by irradiation. The patient experienced renal failure and became dependent on haemodialysis. In 1999, large plasmacytomas developed in the abdomen and left humerus. The abdominal tumour appeared to induce gastroduodenal ulcers and jejunal obstruction. We initiated irradiation therapy without chemotherapy to prevent further growth of the plasmacytoma, although treatment-resistant gastroduodenal ulcers developed. Continued blood loss from the gastroduodenal ulcers resulted in a deterioration in the patient's health, which prevented successful haemodialysis. An autopsy showed that the plasmacytoma had undergone coagulation necrosis. We conclude that the use of combination chemotherapy with topical irradiation was an acceptable treatment measure against IgD plasmacytoma; irradiation without chemotherapy was the most likely cause of the coagulation necrosis seen in the plasmacytoma at autopsy.

Beyond the obvious step of limiting use of non-steroidal anti-inflammatory drugs (NSAIDs), the treatment of ulcers induced by NSAIDs remains controversial. We evaluated the efficacy of the proton-pump inhibitor lansoprazole on NSAID-induced ulcers. Ulcers were endoscopically diagnosed in 47 NSAID users. These patients received 30 mg/day lansoprazole, orally, for 6 or 8 weeks (6 weeks for duodenal ulcers and 8 weeks for other ulcers). Ulcer healing was assessed using an established classification system. The presence of immunoglobulin G antibody against Helicobacter pylori was also evaluated. The antibody was present in the sera of 51% of patients (24/47). Most of the ulcers reached scarring stages S1 (healing) or S2 (good healing), and the S2 healing rate was 35%. Two H. pylori seropositive patients did not reach these stages; their ulcers were improved by H. pylori eradication therapy, followed, in one case, by medication with misoprostol. Lansoprazole seemed to be useful for most patients with NSAID-induced ulcers, but a few needed additional treatments.

A 59-year-old patient with schizophrenia developed Sjögren's syndrome. She also presented with the lupus anticoagulant attributed to long-term medication with chlorpromazine. Serial plasmapheresis treatments were performed to decrease the anti-coagulant activity. As a result, the activated partial thromboplastin time was temporarily improved, but the lupus anti-coagulant activity did not change. Because of her unstable emotional state, she continued to require chlorpromazine, but took a low dose of aspirin (87 mg/day) and never manifested any signs of thrombotic events. In view of the potential anti-thrombotic effects of chlorpromazine, it may not be necessary to use plasmapheresis in an attempt to reduce anti-coagulant activity among patients with chlorpromazine-induced lupus anti-coagulant.

Despite many suicidal cases in patients with systemic lupus erythematosus (SLE), literature on this subject is lacking. To elucidate and prevent this phenomenon, we re-evaluated the clinical records of seven suicidal patients with SLE. Six patients had photosensitivity and insomnia. At the time of the suicide attempt, hypocomplementemia was observed in five of six patients. Diffuse slowing on electroencephalograms were observed in four of five patients. One patient successfully committed suicide while on no therapy while five patients made their attempts under the tapering courses of steroids. Five patients manifested psychoses whereas two patients displayed no psychotic findings. All patients attempted suicide shortly after admission (mean time 20 days). The subsequent courses of the survivors who received more medication were favorable. Therefore, it appears that disease activity was not fully controlled in these patients. Furthermore, signs of an imminent suicide attempt were missed in some cases. Psychosis, insomnia, history of photosensitivity, an incompletely controlled disease state, receiving tapering steroid dose, diffuse slowings on electroencephalograms and the presence of hypocomplementemia appeared to be risks for attempting suicide in SLE. We would recommend that such patients be under psychiatric care for at least 2 months to prevent suicide. When the patient is still psychotic or unstable, further medical care will be required.